Evidence map›Paper›PMID 23053476›Full record

ArticlePflugers Archiv : European journal of physiology2012

The influence of high glucose on the aerobic metabolism of endothelial EA.hy926 cells.

Agnieszka Koziel, Andrzej Woyda-Ploszczyca, Anna Kicinska, Wieslawa Jarmuszkiewicz

Open access · hybridAbstract read
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

51 citing papers in PubMed, 88 citations in OpenAlex.

  1. Article
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  6. Infection and immunity · 2024
    Article
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  18. Review
  19. Metabolic Reprogramming in Tumor Endothelial Cells.International journal of molecular sciences · 2022
    Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Agnieszka KozielDepartment of Bioenergetics, Adam Mickiewicz University, Umultowska 89, Poznan, Poland.
Andrzej Woyda-Ploszczyca
Anna Kicinska
Wieslawa Jarmuszkiewicz
Adam Mickiewicz University in Poznań · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The endothelium is considered to be relatively independent of the mitochondrial energy supply. The goals of this study were to examine mitochondrial respiratory functions in endothelial cells and isolated mitochondria and to assess the influence of chronic high glucose exposure on the aerobic metabolism of these cells. A procedure to isolate of bioenergetically active endothelial mitochondria was elaborated. Human umbilical vein endothelial cells (EA.hy926 line) were grown in medium containing either 5.5 or 25 mM glucose. The respiratory response to elevated glucose was observed in cells grown in 25 mM glucose for at least 6 days or longer. In EA.hy926 cells, growth in high glucose induced considerably lower mitochondrial respiration with glycolytic fuels, less pronounced with glutamine, and higher respiration with palmitate. The Crabtree effect was observed in both types of cells. High glucose conditions produced elevated levels of cellular Q10, increased ROS generation, increased hexokinase I, lactate dehydrogenase, acyl-CoA dehydrogenase, uncoupling protein 2 (UCP2), and superoxide dismutase 2 expression, and decreased E3-binding protein of pyruvate dehydrogenase expression. In isolated mitochondria, hyperglycaemia induced an increase in the oxidation of palmitoylcarnitine and glycerol-3-phosphate (lipid-derived fuels) and a decrease in the oxidation of pyruvate (a mitochondrial fuel); in addition, increased UCP2 activity was observed. Our results demonstrate that primarily glycolytic endothelial cells possess highly active mitochondria with a functioning energy-dissipating pathway (UCP2). High-glucose exposure induces a shift of the endothelial aerobic metabolism towards the oxidation of lipids and amino acids.

Indexed as

Acyl-CoA DehydrogenasesCell LineCell RespirationEndothelial CellsFatty AcidsGlucoseGlutamineHexokinaseHumansIon ChannelsL-Lactate DehydrogenaseMitochondriaMitochondrial ProteinsOxidation-ReductionPalmitatesReactive Oxygen SpeciesAcyl-CoA Dehydrogenasescoenzyme Q10Fatty AcidsGlucoseGlutamineHexokinaseIon ChannelsL-Lactate DehydrogenaseMitochondrial ProteinsPalmitatesReactive Oxygen SpeciesSuperoxide DismutaseSuperoxide Dismutase 2UbiquinoneUCP2 protein, humanUncoupling Protein 2

Identifiers

PMID23053476
PMCPMC3513600
OpenAlexW2023461657

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.